Decitabine Induced Transient Cardiomyopathy: A Case Report

Case Report A 75-yr-old gentleman, with a past medical history of diabetes mellitus and Acute Myeloid Leukemia presented to our emergency department with a chief complaint of exertional dyspnea and chest pain. A week prior to this visit, he had recieved a cycle of decitabine chemotherapy at 20 mg/metered square for ten days. This was his second cycle of decitabine. His out patient medications included megesterol, omeprazole, morphine sulfate and insulin glargine. The patient was admitted to the Coronary Care Unit for Acute Coronary Syndrome. His cardiac enzymes were elevated (peak troponin 30 ng/mL, CKMB 67.4 ng/mL). His 12 lead EKG revealed sinus tachycardia with a ventricular rate of 113, but without acute ST–T wave changes. The BNP was 259 pg/mL. A 2D echo revealed moderate diffuse hypokinesis with an EF of 35%. He subsequently underwent a left heart catheterization, which showed non-obstructive CAD. In our patient, the elevated troponins (peak troponin 30 ng/mL) and BNP were seen concomitant with the onset of cardiogenic shock. Two months ago, his 2 D echocardiogram revealed an ejection fraction of about 55%–65% with slightly increased left ventricular (LV) wall thickness. Discussion The most common adverse effects of decitabine include cytopenia, nausea, pain and erythema/nodules at the injection site. To date, there has been only one reported case of a hypomethylating agent inducing acute myocarditis. We a present a case of reversible, non-ischemic cardiomyopathy secondary to decitabine chemotherapy, which resolved after the drug was discontinued. Trials involving decitabine for the treatment of MDS reported no myocarditis. In our case, the diagnosis of transient cardiomyopathy was highly probable since the patient's troponins and echocardiogram returned to baseline after discontinuation of treatment. Also, the patient never had any further chest pain at his 6 month follow up. In this case, we believe that the elevated Troponin I levels, along with a cardiac catheterization revealing patent coronary vessels, favor our hypothesis that our patient suffered from acute myocarditis as a result of direct toxicity from decitabine chemotherapy. We doubt that there was an underlying infectious etiology, since the patient had three negative blood cultures, two negative urine cultures and a negative viral serology. Our case demonstrates that chest pains in a patient treated with hypomethylating agents should be further explored in order to rule out acute myocarditis

Neutrophil lymphocyte ratio significantly improves the Framingham risk score in prediction of coronary heart disease mortality: insights from the National Health and Nutrition Examination Survey-III.

BACKGROUND: Neutrophil lymphocyte ratio (NLR) has been shown to predict cardiovascular events in several studies. We sought to study if NLR predicts coronary heart disease (CHD) in a healthy US cohort and if it reclassifies the traditional Framingham risk score (FRS) model. METHODS: We performed post hoc analysis of National Health and Nutrition Examination Survey-III (1998-94) including subjects aged 30-79 years free from CHD or CHD equivalent at baseline. Primary endpoint was death from ischemic heart disease. NLR was divided into four categories:4.5. Statistical analyses involved multivariate Cox proportional hazards models as well as discrimination, calibration and reclassification. RESULTS: We included 7363 subjects with a mean follow up of 14.1 years. There were 231 (3.1%) CHD deaths, more in those with NLR\u3e4.5 (11%) compared to NLR4.5 was 2.68 (95% CI 1.07-6.72, p=0.035). There was no significant improvement in C-index (0.8709 to 0.8713) or area under curve (0.8520 to 0.8531) with addition of NLR to FRS model. Model with NLR was well calibrated with Hosmer-Lemeshow chi-square of 8.57 (p=0.38). Overall net reclassification index (NRI) was 6.6% (p=0.003) with intermediate NRI of 10.1% (p CONCLUSIONS: NLR can independently predict CHD mortality in an asymptomatic general population cohort. It reclassifies intermediate risk category of FRS, with significant upward reclassification. NLR should be considered as an inflammatory biomarker of CHD

Perioperative hematoma with subcutaneous ICD implantation: Impact of anticoagulation and antiplatelet therapies

BackgroundThe safety of perioperative anticoagulation (AC) and antiplatelet (AP) therapy with subcutaneous implantable cardioverter‐defibrillator (S‐ICD) implantation is unknown. The purpose of this study was to identify the risk factors associated with hematoma complicating S‐ICD implantation.MethodsRecords were retrospectively reviewed from 200 consecutive patients undergoing S‐ICD implantation at two academic medical centers. A hematoma was defined as a device site blood accumulation requiring surgical evacuation, extended hospital stay, or transfusion.ResultsAmong 200 patients undergoing S‐ICD implantation (age 49 ± 17 years, 67% men), 10 patients (5%) had a hematoma, which required evacuation in six patients (3%). Warfarin was bridged or uninterrupted in 12 and 13 patients, respectively (6% and 6.5%). Four of 12 patients with warfarin and bridging AC (33%) and two of 13 patients with uninterrupted warfarin (15%) developed a hematoma. Neither of the two patients with uninterrupted DOAC had a hematoma. No patients on interrupted AC without bridging (n = 26, 13 with warfarin, 13 with DOAC) developed a hematoma. A hematoma was also more likely with the use of clopidogrel (n = 4/10 vs 10/190, 40% vs 5.3%, P < 0.0001) in combination with aspirin in 12/14 patients. Any bridging AC (odds ratio [OR] 10.3, 1.8–60.8, P = 0.01), clopidogrel (OR 10.0, 1.7–57.7, P = 0.01), and uninterrupted warfarin without bridging (OR 11.1, 1.7–74.3, P = 0.013) were independently associated with hematoma formation.ConclusionAC and/or AP therapy with clopidogrel appears to increase the risk for hematoma following S‐ICD implantation. Interruption of AC without bridging should be considered when it is an acceptable risk to hold AC.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/145383/1/pace13349_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/145383/2/pace13349.pd

CASE REPORT Anomalies Associated With Congenitally Corrected Transposition of Great Arteries: Expect the Unexpected.

OBJECTIVE: Congenitally corrected transposition of great arteries (CCTGA) is characterized by atrioventricular and ventriculoarterial discordance. Characterizations of these anomalies are important because they may influence surgical approach and management. METHODS: We present a case of newly diagnosed CCTGA at the age of 50. He presented with sudden onset of shortness of breath for the first time and was diagnosed with CCTGA. Echocardiogram, magnetic resonance imaging, and cardiac catheterization were utilized to elucidate the pathology. RESULTS: Intraoperatively, patient\u27s CCTGA and ventricularization of the right ventricle were confirmed. The severe systemic atrioventricular valve regurgitation was replaced with a bioprosthetic valve (Medtronic Mosaic No. 29) with placement of epicardial ventricular leads for possible future placement of automatic implantable cardioverter defibrillators. Pathology report confirmed a degeneration of the systemic atrioventricular valve. CONCLUSIONS: Significant coronary artery anomalies have also been described in literature with CCTGA. The variances encountered in this case are excellent examples of the intricacies associated in diagnosis and surgical care in patients with CCTGA